Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/43484
Título: Acetyl derivative of quercetin 3-methyl ether-induced cell death in human leukemia cells is amplified by the inhibition of ERK
Autores/as: Rubio Sánchez, Sara 
Quintana Aguiar, José Martín 
Eiroa, José L. 
Triana, Jorge
Estévez Rosas, Francisco Jesús 
Clasificación UNESCO: 32 Ciencias médicas
Palabras clave: Activated Protein-Kinase
P38 Map Kinase
Induced Apoptosis
Cancer-Therapy
Molecular-Mechanisms, et al.
Fecha de publicación: 2007
Editor/a: 0143-3334
Proyectos: Nuevos Compuestos Antileucémicos 
Publicación seriada: Carcinogenesis 
Resumen: Flavonoids are polyphenolic compounds that are ubiquitously in plants and display a vast array of biological activities. Here we have studied the effect of the phenylbenzo-γ-pyrone-derivative quercetin 3-methyl ether tetracetate (QD), obtained by acetylation of the natural product quercetin 3-methyl ether, on cell viability of human leukemia HL-60 and U937 cell lines. The results show that QD was cytotoxic and induced G 2 –M phase cell cycle arrest on both cell lines and it was a potent apoptotic inducer on HL-60 cells. QD-induced apoptosis is (i) mediated by caspase activation, since it was prevented by the non-specific caspase inhibitor z-VAD-fmk, (ii) associated with cytochrome c release and (iii) triggered in Bcl-2 over-expressing U937 cells. The treatment of HL-60 and U937 cells with QD also induces the activation of the mitogen-activated protein kinases (MAPKs) pathway, including c-Jun N-terminal kinase, p38 mitogen-activated protein kinase and extracellular signal-regulated kinases (ERK) 1/2. Inhibition of c-Jun N-terminal kinase by SP600125 and of p38 mitogen-activated protein kinase by SB203580 had no influence on QD-mediated apoptosis. In contrast, inhibition of ERK1/2 with the pharmacologic inhibitors U0126 or PD98059, together with QD, resulted in an important enhancement of apoptosis. Cells are sensitized to QD-mediated apoptosis after blocking ERK1/2, which suggests that inhibition of this pathway is a valuable strategy to increase the sensitivity of human leukemia HL-60 cells toward QD.
URI: http://hdl.handle.net/10553/43484
ISSN: 0143-3334
DOI: 10.1093/carcin/bgm131
Fuente: Carcinogenesis [ISSN 0143-3334], v. 28, p. 2105-2113
Colección:Artículos
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